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Anxiety has been linked to shortened telomeres, markers of biological aging. A study found that phobic anxiety was associated with shorter telomeres in middle-aged and older women. Shortened telomeres increase the risk of diseases like cancer, heart disease, and dementia. Understanding the relationship between psychological stress and telomere length provides insight into how anxiety may lead to premature aging at the cellular level. Studying centromere structure helps explain errors in cell division that can cause genetic diseases.
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Anxiety Linked to Shortened Telomeres And Cell Division: Puzzling Findings Re...
This document summarizes recent findings relating to telomeres, centromeres, and their connection to anxiety and cell division. Specifically, it was found that: 1) anxiety is linked to shortened telomeres in middle-aged and older women, increasing risks of disease and early mortality, and 2) while centromeres were thought to contain a single Cse4 protein, live cell imaging revealed there are actually two Cse4 molecules interacting at the centromere during cell division. Understanding centromere structure is important for genomic integrity and detecting genetic diseases from cell division errors.
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NEWS ABOUT TELOMERES
Telomeres play an important role in cellular aging and division. A study found that women with phobic anxiety had shorter telomeres, suggesting anxiety is a risk factor for accelerated aging. In cancer cells, telomerase remains active, allowing indefinite division by regenerating telomeres. Researchers discovered a protein complex that normally inhibits telomerase; in cancer it is delayed, allowing telomerase to extend telomeres and confer immortality. Understanding these processes may lead to new prevention and treatment strategies for diseases of aging and cancer.
Biologia molecular Laura Cuartas Q
Lem4 is a protein that coordinates the activity of kinases and phosphatases on target proteins essential for cell division. It plays an important role in ensuring the nuclear envelope disappears and reassembles correctly during cell division. Telomeres and the telomerase enzyme are involved in cell aging and linked to increased cancer risk if telomeres are shortened. Stress and anxiety can negatively impact telomere length through emotional responses.
Hani hamed dessoki, telomeres and depression
A new study found that people who had experienced depression had significantly shorter telomeres, representing about 4 to 6 years of accelerated aging at the cellular level. Telomeres are structures at the end of chromosomes that protect DNA from damage. Shorter telomeres have been linked to aging. The study of over 2,400 people showed that those with a history of depression had telomeres about 83 to 84 base pairs shorter than those without depression, even after accounting for other lifestyle factors. While the study did not prove cause and effect, depression is known to disrupt many physical systems, and these findings suggest psychological distress from depression may lead to accelerated biological aging.
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Seminar Summaries
Dr Kad's talk summarized his lab's work using single molecule approaches to study nucleotide excision repair in prokaryotes. While prokaryotic nucleotide excision repair involves only 6 proteins compared to 30+ in eukaryotes, the interactions between the 6 proteins are complex. His lab uses DNA "tightropes" stretched between beads to observe individual repair protein interactions, finding that the UvrA protein does not slide along DNA as expected but instead binds and dissociates across the strand, while UvrAB complex slides to scan for damage.
Interesting medical news presentation
Here I show to you very interesting research news and medical utility. We can see the future of the epigenetics and molecular medicine.
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Alejo Rodriguez-Fraticelli, from Dr Fernando Martin-Belmonte’s laboratory in the CBMSO in Spain, has recently published with co-workers a paper in the Journal of Cell Biology in which they describe their approach to epithelial cells morphogenesis and uncover the role of cell confinement on epithelial polarity via peripheral actin contractility. The team sheds light on a phenomenon that is crucial to understand the physiology of the organs, but also the mechanisms underlying the development and progression of agressive epithelial cancers.
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James_Fitch_Poster Presentation
This study analyzed microhemorrhages (MH) in brain tissue samples from individuals with Down syndrome (DS), Alzheimer's disease (AD), and DS with AD, compared to age-matched controls. Brain tissue was stained to identify iron-rich MH near blood vessels. MH counts were significantly higher in samples from individuals with DS/AD compared to all other groups, as well as higher in AD samples compared to controls. The results suggest cerebrovascular dysfunction may contribute to brain aging in DS, and that DS combined with AD further increases MH counts more than AD alone.
Muthusamy_et_al-2015-Aging_Cell
This study demonstrates that the protein MARCKS is important for maintaining the functions and barrier integrity of ependymal cells (ECs) in the brain as they age. ECs form a barrier between cerebrospinal fluid and brain tissue. The study found that MARCKS and related proteins are highly polarized in young ECs but lose their polarization as ECs age. Deleting MARCKS in ECs caused accumulation of mucins and lipids inside ECs, disrupting the barrier and inducing inflammation in surrounding brain tissue, mimicking aspects of normal aging. This suggests MARCKS is required for EC functions like mucin clearance and lipid metabolism that decline with aging and impact brain homeostasis.
Cell junctions
Cell junctions are structures that allow for long-term association between neighboring cells. The three main types are tight junctions, adhesive junctions, and gap junctions. Adhesive junctions such as desmosomes and adherens junctions link cells together and to the extracellular matrix. These junctions contain intracellular attachment proteins and transmembrane linker proteins that anchor actin filaments or intermediate filaments. Gap junctions allow direct communication between cells by forming channels between their plasma membranes.
Stem cell research in Parkinson's Disease
Stem cell research shows promise for treating Parkinson's disease. Studies have found that transplanting embryonic stem cells or neural stem cells into animal models of Parkinson's can reduce symptoms by generating new dopamine-producing cells. However, many of these transplanted cells have failed to maintain their function over time or have caused tumor formation. A clinical trial in Peru found that transplanting bone marrow-derived stem cells into the brains of Parkinson's patients improved their symptoms, but long-term data is still needed. Future research aims to develop safer and more effective stem cell therapies by improving protocols and understanding how to support long-term cell survival and specialization without tumor risks.
Cell junctions 2013
This document discusses cell junctions and their roles in various biological processes. It defines the main types of cell junctions, including tight junctions, gap junctions, focal adhesions, adherens junctions, and desmosomes. It provides examples of how cell junction gene expression changes during epithelial-to-mesenchymal transition, stem cell differentiation, cancer, atopic dermatitis, and the effects of probiotic bacteria on intestinal barriers. PCR array tools are presented as ways to study cell junctions and related pathways at the gene expression level to better understand their functions in normal and disease states.
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The document presents a hypothetical model of biomarkers for Alzheimer's disease progression. It proposes that:
1) Abnormal amyloid beta processing occurs first, before symptoms, which is detected by reduced CSF Aβ42 and increased amyloid PET tracer retention.
2) After a lag period, neuronal dysfunction and neurodegeneration become dominant, detected by increased CSF tau and brain atrophy on structural MRI.
3) Neurodegeneration is accompanied by synaptic dysfunction detected by decreased fluorodeoxyglucose uptake on PET.
4) The model relates disease stage to biomarkers, with amyloid biomarkers becoming abnormal first before neurodegenerative biomarkers and symptoms, which then correlate with severity.
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This document discusses various materials and therapies for peripheral nerve regeneration. It covers guidance therapies using nerve conduits made from natural and synthetic biomaterials. Biomolecular therapies involve delivering growth factors to promote regeneration. Cellular therapies utilize Schwann cells, stem cells, and genetically modified cells. Advanced techniques include nerve conduits fabricated using 3D printing, injection molding and aligned polymer fibers. Future areas of focus are multi-chamber conduits and stem cell therapies to further enhance regeneration.
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Tight junctions play an important role in regulating gene expression and cell proliferation. Two key proteins, ZO-1 and ZO-2, shuttle between the tight junctions and the nucleus in proliferating cells. ZO-1 expression is higher in contact-inhibited cells and suppresses proliferation. ZO-2 localizes to nuclear speckles in proliferating cells to regulate pre-mRNA splicing. The nuclear transport of these proteins allows tight junctions to influence gene transcription and cell cycle progression.
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This document summarizes adult neurogenesis and its role in brain disorders such as Alzheimer's disease. It describes how new neurons are generated from neural stem cells in the subventricular zone and hippocampus of the adult brain. Alterations in neurogenesis are linked to neurological conditions like Alzheimer's, where neurofibrillary tangles and amyloid plaques accumulate and neurons die, affecting areas like the hippocampus early on. Efforts are underway to understand how neurogenesis contributes to disease and potentially harness neural stem cells to help repair symptoms.
Method for physiologic phenotype characterization at the single-cell level in...
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under normoxic and hypoxic conditions. It is based on real-time concentration measurements of metabolites of
interest by means of extracellular optical sensors in cell-isolating microwells of subnanoliter volume. We present the results of a series of measurements of oxygen consumption rates (OCRs) of individual non-interacting and interacting human epithelial cells. We measured the effects of cell-to-cell interactions by using the system’s capability to isolate two and three cells in a single well. The major advantages of the approach are: 1. ratiometric, intensity-based characterization of the metabolic phenotype at the single-cell level, 2. minimal invasiveness due to the distant positioning of sensors, and 3. ability to study the effects of cell-cell interactions on cellular respiration rates.
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NEWS ABOUT TELOMERES
Telomeres play an important role in cellular aging and division. A study found that women with phobic anxiety had shorter telomeres, suggesting anxiety is a risk factor for accelerated aging. In cancer cells, telomerase remains active, allowing indefinite division by regenerating telomeres. Researchers discovered a protein complex that normally inhibits telomerase; in cancer it is delayed, allowing telomerase to extend telomeres and confer immortality. Understanding these processes may lead to new prevention and treatment strategies for diseases of aging and cancer.
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Telomeres
Telomeres are repetitive DNA sequences located at the ends of chromosomes that protect genetic material during cell division. As cells divide, telomeres slowly shorten due to the inability of DNA replication to fully copy chromosome ends. Eventually telomeres become so short that cells can no longer divide, leading to cellular aging. In most human cells, the enzyme telomerase is turned off, contributing to telomere shortening with each cell division. However, telomerase is active in approximately 90% of cancer cells, allowing them to divide indefinitely and overcome the natural limits of cellular replication. Telomere shortening may promote cancer by causing chromosome instability when telomeres become dysfunctional. Maintaining telomere length through telomerase
ROLE OF TELOMERE AND IN CELL AGEING
Telomeres play an important role in cellular aging. Telomeres are nucleoprotein structures located at the end of chromosomes that protect chromosomal DNA from deterioration. With each cell division, telomeres shorten due to the end-replication problem. When telomeres become too short, cells enter a permanent non-dividing state called senescence. Telomere shortening has thus been proposed as a molecular clock that counts the number of cell divisions and limits the replicative capacity of cells, contributing to aging at the cellular and organismal level. Telomerase is an enzyme that can add telomeric repeats to chromosome ends and counteract telomere shortening. Dysfunctional telomeres and telomerase
G e N e t i c S , t e c H N o l o G Y , A N D S o c i e t .docx
G e N e t i c S , t e c H N o l o G Y , A N D S o c i e t Y 289
G e n e t i c s , t e c h n o l o G y , a n d s o c i e t y
telomeres: the Key to immortality?
Humans, like all multicellular organisms, grow old and die. As we age, our immune
systems become less efficient, wound
healing is impaired, and tissues lose re-
silience. It has always been a mystery why
we go through these age-related declines
and why each species has a characteris-
tic finite life span. Why do we grow old?
Can we reverse this march to mortality?
Some recent discoveries suggest that the
answers to these questions may lie at the
ends of our chromosomes.
The study of human aging begins with
a study of human cells growing in culture
dishes. Like the organisms from which the
cells are taken, cells in culture have a fi-
nite life span. This replicative senescence
was first noted by Leonard Hayflick in
the 1960s. He reported that normal hu-
man fibroblasts lose their ability to grow
and divide after about 50 cell divisions.
These senescent cells remain metaboli-
cally active but can no longer prolifer-
ate. Eventually, they die. Although we
don’t know whether cellular senescence
directly causes organismal aging, the evi-
dence is suggestive. For example, cells de-
rived from young people undergo more
divisions than those from older people;
cells from short-lived species stop grow-
ing after fewer divisions than those from
longer-lived species; and cells from pa-
tients with premature aging syndromes
undergo fewer divisions than those from
normal patients.
Another characteristic of aging cells
involves their telomeres. In most mam-
malian somatic cells, telomeres become
shorter with each DNA replication be-
cause DNA polymerase cannot synthe-
size new DNA at the ends of each parent
strand. However, as discussed in detail in
this chapter, cells that undergo extensive
proliferation, like embryonic cells, germ
cells, and adult stem cells, maintain their
telomere length by using telomerase—a re-
markable RNA-containing enzyme that
adds telomeric DNA sequences onto the
ends of linear chromosomes. However,
most somatic cells in adult organisms do
not proliferate and do not contain active
telomerase.
Could we gain perpetual youth and vi-
tality by increasing our telomere lengths?
Studies suggest that it may be possible to
reverse senescence by artificially increas-
ing the amount of telomerase in our cells.
When investigators introduced cloned
telomerase genes into normal human
cells in culture, telomeres lengthened,
and the cells continued to grow past their
typical senescence point. These studies
suggest that some of the atrophy of tis-
sues that accompanies old age could be
reversed by activating telomerase genes.
However, before we use telomerase to
achieve immortality, we need to consider
a potential serious side effect: cancer.
Although normal cells shorten their
telomeres and undergo senescence after
a specific num ...
Cell ageing ty
This document discusses cellular aging and theories of aging. It covers several key points:
1) Cellular senescence and the Hayflick limit, where cells stop dividing after a certain number of divisions.
2) Theories of aging including the free radical theory, somatic mutation theory, and telomere loss theory.
3) Types of cell death including apoptosis, necrosis, necroptosis, and pyroptosis. Programmed cell death limits inflammation while necrosis causes damage and inflammation.
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A group collaborative effort of independent research pooled together to answer the question of why we age.
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Najaf bio 4 4 (2)
Chromosomes contain DNA and are found in pairs in eukaryotic cells like humans who have 23 chromosome pairs. Genes are segments of DNA that control traits and can exist in different forms called alleles. Mutations are random changes in genetic material that can cause conditions like sickle cell anemia. Meiosis produces gametes with half the normal chromosome number through two cell divisions followed by crossing over and separation of homologous chromosomes. Genetic engineering techniques like polymerase chain reaction and DNA profiling allow manipulation and analysis of DNA.
Telomerase its role in aging and cancer
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal DNA from degradation. Telomerase is an enzyme that adds telomere repeats to the ends of chromosomes to overcome replication-induced shortening. In normal cells, telomerase is inactive and telomeres shorten with each cell division, eventually leading to senescence. Cancer cells maintain telomere length through telomerase reactivation, allowing unlimited proliferation. Studies found telomerase expressed in 90% of human tumors but not normal tissues, supporting its role in immortality.
Aging and the telomere connection dr. Jerry w. Shay - april 2012
1. Telomeres are repetitive DNA sequences at the ends of chromosomes that protect chromosomal DNA from deterioration. Each cell division, telomeres shorten until they reach a critical length that causes cells to stop dividing.
2. Short telomere length is associated with aging and age-related diseases by limiting tissue regeneration abilities. Telomere length measurements provide insight into overall health and longevity.
3. Environmental stressors like smoking can accelerate telomere shortening, while behaviors like exercise may help slow the rate of shortening. Quantitative telomere tests are being developed to monitor health and the effects of therapies on telomere biology.
BIOMOL
Stem cell populations reside in niches within organs that control when stem cells replicate or produce daughter cells. A study in fruit flies found that the division of stem cells in testes is regulated at the final stage of replication before daughter cells separate. Previous studies showed different stem cell types in the fruit fly testis niche had to coordinate to properly make sperm. Advances in understanding stem cell replication and DNA damage repair could enable greater progress in tissue regeneration and gene therapy.
Cell Division -Mitosis -XI Biology- Tarini.pptx
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About Tolemerase
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect cellular DNA from degradation. Telomere shortening is linked to cellular aging and is thought to be a root cause of age-related diseases. Telomerase is an enzyme that adds telomere repeats to chromosome ends and counteracts telomere shortening during cell division. Studies have shown that activating telomerase can prolong cellular lifespan, rejuvenate cells, and delay age-related changes in animals. Preliminary studies in humans using TA-65, a molecule that activates telomerase, have shown benefits such as reduced levels of senescent immune cells and lengthened short telomeres without safety issues.
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The document provides an overview of nuclear structure and function. It discusses the nucleus, nuclear envelope, nucleolus, chromatin, DNA replication and transcription processes. It describes chromosomal structure including centromeres, telomeres, and histones. It covers chromosomal abnormalities like deletions, duplications, inversions, insertions, and translocations. It discusses the Philadelphia chromosome translocation in CML cells. It also summarizes chromosomal karyotyping, the cell cycle phases of interphase and cell division, and mitosis and cytokinesis.
Cell Mechanisms Presentation.pdf
This document provides an overview of a presentation on cell mechanisms that covers four main topics:
1) The mechanisms that confine cells and tissues to specific anatomical sites through intercellular adhesion and memory.
2) Four types of cellular adaptations.
3) A comparison of necrosis and apoptosis, the two main types of cell death. Necrosis is unregulated cell death that causes inflammation, while apoptosis is a regulated process of cell suicide.
4) At least 20 slides are required to be created in PowerPoint or Impress covering these topics using at least four scholarly sources.
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Plegable aleja
- 1. Anxiety Linked to Shortened Telomeres And Cell Division: Puzzling Findings Relating to Centromere Structure Reconciled Alejandra Henao Buitrago Medical student
- 2. FOLDING
- 3. FOLDING
- 4. INTRODUCTION Understanding Telomeres are centromeres is critical considered markers of because of the role biological or cellular they play in maintaining aging. genomic integrity.
- 5. Cell Division: Puzzling Findings Relating To Centromere Structure Reconciled Science Daily (July 19, 2012)
- 6. Cell Division: Puzzling Findings Relating To Centromere Structure Reconciled A nucleosome, a short coil of DNA twisted around a core of proteins forms at each centromere. Within the core is a protein, called Cse4 in yeast. But the overall architecture of that nucleosome was unknown. has used live cell imaging to reveal constituents of the centromeric protein core.
- 7. Cell Division: Puzzling Findings Relating To Centromere Structure Reconciled • Two methods were combined to probe yeast cells engineered to express Cse4 hooked to a green fluorescent protein (GFP) tag. • The approach allowed them to track and then count in a living cell the number of Cse4 molecules in a centromeric nucleosome. • Yeast cells have 16 chromosomes, each with one centromere. If each centromere contained just one copy of Cse4, then the dot glowing in each cell should be 16 times brighter than a single GFP molecule.
- 8. Cell Division: Puzzling Findings Relating To Centromere Structure Reconciled Was found that two evidence molecules of Cse4 were interacting at the centromere in anaphase, but these interactions were not present during the rest of the cell cycle. Is concluded that the timing of structural changes differs in yeast and human cells, But that human and yeast centromeres undergo similar dynamic changes with the cell cycle.
- 9. Comment know the functioning of the centromere is important for understanding the segregation of chromosomes and of the consequences of errors in cell division.
- 10. Anxiety Linked to Shortened Telomeres, Accelerated Aging ScienceDaily (July 11, 2012)
- 11. Anxiety Linked to Shortened Telomeres, Accelerated Aging
- 12. Anxiety Linked to Shortened Telomeres, Accelerated Aging A new study shows that a phobic anxiety was associated with shorter telomeres in middle aged and older women.
- 13. Anxiety Linked to Shortened Telomeres, Accelerated Aging Shortened telomeres have been linked to increased risk of cancers, heart disease, dementia and mortality. This study is notable for showing a connection between a common form of psychological stress, phobic anxiety, and a plausible mechanism for premature aging.
- 14. Comment See the relationship between a psychological stress with premature aging, is important to give appropriate diagnostic, provide timely treatment using the
- 15. MEDICAL UTILITY
- 16. MEDICAL UTILITY Most cells in the adult exhibit only limited telomerase activity, meaning that as cells divide and replicate their DNA, the chromosomes’ telomeres become shorter. This limits the number of times a cell can divide and contributes to aging.
- 17. MEDICAL UTILITY Longer telomeres are hypothesized to correlate with improved longevity and reduced disease burden.
- 18. MEDICAL UTILITY The study of centromere helps detect genetic diseases when there are errors in cell division
- 19. BIBLIOGRAPHY MARTINEZ S, Lina María, Biología molecular, 7 ed. Medellín: UPB. Fac de Medicina , 2012. 69-70 p. WATSON, James, Biología molecular del Gen, 5 ed. Buenos Aires, Madrid, ed panamericana, 2006. 151-153 p.